T cells are immune cells comprising up 70 to 80% of peripheral blood lymphocytes, and are widely distributed in the spleen and lymph nodes throughout the body to contribute to biological defense. T cells are such cells expressing a T cell antigen receptor (T cell receptor; TCR) on the surface thereof, and play the center role in acquired immune system. Activation of T cells is caused when a TCR on the T cell membrane recognizes a major histocompatibility complex (MHC)+an antigen presented by an antigen-presenting cell. One T cell expresses only one type of antigen-specific TCR, thereby exerting an immune response specific to every antigen. Further, T cells express a CD4 or CD8 molecule on the surface thereof, and therefore are classified into the CD4-positive T cell subset and the CD8-positive T cell subset, which form totally different cell populations with different immune functions. The CD4-positive T cell subset is called “helper T cell”, and has functions to induce to express the functions of other T cells and to cause differentiation of a B cell into an antibody-producing cell. Meanwhile, the CD8-positive T cell subset is called “killer T cell”, and has the function to destroy virus-infected cells, cancer cells, etc. and is involved in rejection, which is a problem at the time of organ transplantation. Further, from a functional standpoint, helper T cells are further classified into 4 subgroups (Th1 cell, Th2 cell, Th17 cell and Treg cell). The Th1 cell is an effector cell differentiated mainly in the presence of IL-l2, and mainly produces IFN-γ to induce cellular immunity, which is involved in autoimmune disease and delayed-type allergy. The Th2 cell is an effector cell differentiated mainly in the presence of IL-4, and mainly produces IL-4 to induce humoral immunity, which is involved in immediate-type allergy. The Th17 cell is a recently-identified subgroup. It is believed that the Th17 cell is differentiated in the presence of IL-6 or TGF-β to produce IL-17, which is functionally involved in autoimmune disease. The Treg cell is a CD4-positive T cell that is CD25-positive, which is called “regulatory T cell”, and controls immune reaction to contribute to maintenance of homeostasis of the immune system. Thus, T cells play an important role in any pathological condition that involves immunity, such as infection disease, tumor, organ transplantation and allergy. Among others, the CD4-positive helper T cell plays a central role in biological defense, including control of other immune cells. On the other hand, excessive immune response of the helper T cell may cause autoimmune disease and allergy disease. That is, appropriate and moderate activation of the helper T cell is essential for maintenance of homeostasis of the immune system.
As a conventional method for controlling T cell immunity, an immunosuppressive agent is frequently used. However, there is a problem that effects of immunosuppressive agents are non-specific to T cell subsets. As typical immunosuppressive agents, cyclosporine and FK506 are known, but these agents suppress activation of all types of the T cells. Steroid-based agents are also widely used for treating autoimmune disease and allergy disease. However, there is a problem that these agents exert effects which are nonspecific to cells and at once have strong side effects. Thus, a method for selective control of a helper T cell function has not been established yet.
Gangliosides are a group of sphingoglycolipids having sialic acid, and all endogenous sphingoglycolipids are biosynthesized from ceramide through a series of enzyme reactions (FIG. 1). GM3 is a molecule that is the origin of all gangliosides, and is synthesized from lactosylceramide by GM3 biosynthetic enzyme (sialic acid transferase I; SAT-I). Gangliosides are expressed in all mammalian cells and constitute a microdomain on the cell membrane called “raft” together with cholesterol and sphingomyelin. According to recent researches, it has been elucidated that the raft functions as an important place for transmitting information from a receptor into the cell (Non-patent document 1). Also in the T cell, the raft provides a place essential for TCR-mediated intracellular signaling. When the raft structure is destroyed using an agent for removing cholesterol from the cell membrane, TCR-mediated signaling is suppressed and the T cell is no longer activated (Non-patent document 2). The functional role of gangliosides in T cell activation has been tested using a method of adding an inhibitor for a biosynthetic enzyme of sphingoglycolipid or an exogenous ganglioside. As a result, however, no significant influence was observed, or various effects were respectively recognized that is caused by adding different gangliosides (Non-patent document 3). In addition, there was no study in which functions of gangliosides with respect to TCR-mediated activation are analyzed in vivo for every T cell subset.    Non-patent document 1: K Simons and D Toomre. Lipid raft and signal transduction. Nat. Rev. Mol. Cell Biol. 1, 31-39, 2000    Non-patent document 2: P. W. Janes, S. C. Ley, A. I. Magee and P. S. Kabouridis. The role of lipid rafts in T cell receptor signaling. Semin. Immunol. 12, 23-34, 2000    Non-patent document 3: M Potapenko, G. V. Shurin and J de Leon. Gangliosides as immunomodulator. Adv. Exp. Med. Biol. 601, 195-203, 2007